Guofeng Cheng

TL;DR: Compound 39 (ledipasvir, GS-5885) has an extended plasma half-life of 37-45 h in healthy volunteers and produces a rapid >3 log viral load reduction in monotherapy at oral doses of 3 mg or greater with once-daily dosing in genotype 1a HCV-infected patients.

TL;DR: The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription in primary human hepatocytes (PHH) as mentioned in this paper.

TL;DR: The current study shows that ledipasvir inhibits NS5A through direct binding and that resistance to ledip asvir is the result of a reduction in binding affinity to NS 5A mutants.

TL;DR: The in vitro pharmacology of a novel C-nucleoside adenosine analog monophosphate prodrug exhibited the potential for potent anti-HCV activity in a proof-of-concept clinical trial, but its utility was limited by the requirement of high dose levels and pharmacokinetic and pharmacodynamic variability.

TL;DR: Given that the adapted phenotype resulted from a combination of mutations in structural and nonstructural proteins, these data suggest that the improved viral titers are likely due to differences in virus particle assembly that result in significantly improved infectious particle stability.